Description:
Hawthorn is a small to midium sized deciduous tree 5 to 15mtr. tall, grows as a hedge plant in Europe but found mostly in temperate regions North America ,Western Asia, India, China and northern Africa.Its flowers are umbrella shaped and clustered white or pink,leaves are glossy green toothed and the berries are bright shiny red. The white coloured flowers are borne in flat-topped inflorescences termed corymbs or globular in inflorescences termed umbels and usually contains 5 petals,5 and 18 stamens and have a rancid oder. the fruits are known as pomes, although the seeds and their bony ndocarps are termed pyrenes. The calyx is present. The throns are small with sharp tipped branches that arise either from other branches or from the trunk, and are typically 1-3 cm long.Hawthorn bark or stem has hardwood ,smooth and ash-grey.CLICK & SEE THE PICTURES..>….(01).......(1).…..(2).

*anti-arrhythmic effects (heart)
*anticoagulant [an agent that prevents the formation of clots in a liquid, as in blood]
*antispasmodic [an agent that relieves or checks spasms or cramps]
*antioxidants [contributing to the oxidation of free radicals which are believed to contribute to premature aging and dementia] that help increase the flow of blood and oxygen to the heart

*helps rid the body of excess salt and water thus supporting weight-loss and weight control programs
*urinary tract infections, combined with Agrimony, Thyme and Golden Rod

Respiratory Tract Conditions

*sore throat

Other Uses:

*an excellent liquor made from Hawthorn berries and brandy
*repels bees and is only pollinated by flies

Hawthorn is best-used long term as the active constituents do not produce rapid results. Benefits develop slowly having a direct effect on the heart itself, especially in cases of heart damage and heart problems associated with liver disease. It is gentle and safe for long-term use with no toxic side effects.

Disclaimer:
The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.

Definition:
The long QT syndrome (LQTS) is a rare inborn heart condition in which delayed repolarization of the heart following a heartbeat increases the risk of episodes of torsade de pointes (TDP, a form of irregular heartbeat that originates from the ventricles). These episodes may lead to palpitations, fainting and sudden death due to ventricular fibrillation. Episodes may be provoked by various stimuli, depending on the subtype of the condition.CLICK & SEE
You can be born with a genetic mutation that puts you at risk of long QT syndrome. In addition, certain medications and medical conditions may cause long QT syndrome.

The condition is so named because of the appearances of the electrocardiogram (ECG/EKG), on which there is prolongation of the QT interval.

Long QT syndrome is treatable. You may need to limit your physical activity, avoid medications known to cause prolonged Q-T intervals or take medications to prevent a chaotic heart rhythm. Some people with long QT syndrome need surgery or an implantable device.

Symptoms :
Many people with long QT syndrome don’t have any signs or symptoms. They may be aware of their condition only from results of an electrocardiogram (ECG) performed for an unrelated reason, because they have a family history of long QT syndrome or because of genetic testing results.

For people who do experience signs and symptoms of long QT syndrome, the most common symptoms include:

*Fainting. This is the most common sign of long QT syndrome. In people with long QT syndrome, fainting spells (syncope) are caused by the heart temporarily beating in an erratic way. These fainting spells may happen when you’re excited, angry or scared, or during exercise. Fainting in people with long QT syndrome can occur without warning, such as losing consciousness after being startled by a ringing telephone.

Signs and symptoms that you’re about to faint include lightheadedness, heart palpitations or irregular heartbeat, weakness and blurred vision. However, in long QT syndrome, such warning signs before fainting are unusual.

*Seizures. If the heart continues to beat erratically, the brain becomes increasingly deprived of oxygen. This can then cause generalized seizures.

*Sudden death. Normally, the heart returns to its normal rhythm. If this doesn’t happen spontaneously and paramedics don’t arrive in time to convert the rhythm back to normal with an external defibrillator, sudden death will occur.Signs and symptoms of inherited long QT syndrome may start during the first months of life, or as late as middle age. Most people who experience signs or symptoms from long QT syndrome have their first episode by the time they reach age 40.

Rarely, signs and symptoms of long QT syndrome may occur during sleep or arousal from sleep.

Causes:
Your heart beats about 100,000 times a day to circulate blood throughout your body. To pump blood, your heart’s chambers contract and relax. These actions are controlled by electrical impulses created in the sinus node, a group of cells in the upper right chamber of your heart. These impulses travel through your heart and cause it to beat.

After each heartbeat, your heart’s electrical system recharges itself in preparation for the next heartbeat. This process is known as repolarization. In long QT syndrome, your heart muscle takes longer than normal to recharge between beats. This electrical disturbance, which often can be seen on an electrocardiogram (ECG), is called a prolonged Q-T interval.

Prolonged Q-T interval
An electrocardiogram (ECG, also called an EKG) measures electrical impulses as they travel through your heart. Patches with wires attached to your skin measure these impulses, which are displayed on a monitor or printed on paper as waves of electrical activity.

An ECG measures electrical impulses as five distinct waves. Doctors label these five waves using the letters P, Q, R, S and T. The waves labeled Q through T show electrical activity in your heart’s lower chambers.

The space between the start of the Q wave and the end of the T wave (Q-T interval) corresponds to the time it takes for your heart to contract and then refill with blood before beginning the next contraction.

By measuring the Q-T interval, doctors can tell whether it occurs in a normal amount of time. If it takes longer than normal, it’s called a prolonged Q-T interval. The upper limit of a normal Q-T interval takes into account age, sex, and regularity and speed of the heart rate.

Long QT syndrome results from abnormalities in the heart’s electrical recharging system. However, the heart’s structure is normal. Abnormalities in your heart’s electrical system may be inherited or acquired due to an underlying medical condition or a medication.

Inherited long QT syndrome
At least 12 genes associated with long QT syndrome have been discovered so far, and hundreds of mutations within these genes have been identified. Mutations in three of these genes account for about 70 to 75 percent of long QT syndrome, and cause the forms referred to as LQT1, LQT2 and LQT3.

Doctors have described two forms of inherited long QT syndrome:

*Romano-Ward syndrome. This more common form occurs in people who inherit only a single genetic variant from one of their parents.

*Jervell and Lange-Nielsen syndrome. Signs and symptoms of this rare form usually occur earlier and are more severe than in Romano-Ward syndrome. It’s seen in children who are born deaf and have long QT syndrome because they inherited genetic variants from each parent.

Additionally, scientists have been investigating a possible link between SIDS and long QT syndrome and have discovered that about 10 percent of babies with SIDS had a genetic defect or mutation for long QT syndrome.

Acquired long QT syndrome
More than 50 medications, many of them common, can lengthen the Q-T interval in otherwise healthy people and cause a form of acquired long QT syndrome known as drug-induced long QT syndrome.

Medications that can lengthen the Q-T interval and upset heart rhythm include certain antibiotics, antidepressants, antihistamines, diuretics, heart medications, cholesterol-lowering drugs, diabetes medications, as well as some antifungal and antipsychotic drugs.

People who develop drug-induced long QT syndrome may also have some subtle genetic defects in their hearts, making them more susceptible to disruptions in heart rhythm from taking drugs that can cause prolonged Q-T intervals.

Risk Factors:People at risk of long QT syndrome include:

*Children, teenagers and young adults with unexplained fainting, unexplained near drownings or other accidents, unexplained seizures, or a history of cardiac arrest

*Family members of children, teenagers and young adults with unexplained fainting, unexplained near drownings or other accidents, unexplained seizures, or a history of cardiac arrest

*Blood relatives of people with known long QT syndrome

*People taking medications known to cause prolonged Q-T intervals

Long QT syndrome often goes undiagnosed or is misdiagnosed as a seizure disorder, such as epilepsy. However, researchers believe that long QT syndrome may be responsible for some otherwise unexplained deaths in children and young adults. For example, an unexplained drowning of a young person may be the first clue to inherited long QT syndrome in a family.

People with low potassium, magnesium or calcium blood levels — such as those with the eating disorder anorexia nervosa — may be susceptible to prolonged Q-T intervals. Potassium, magnesium and calcium are all important minerals for the health of your heart’s electrical system.

Diagnosis:
The diagnosis of LQTS is not easy since 2.5% of the healthy population have prolonged QT interval, and 10–15% of LQTS patients have a normal QT interval. A commonly used criterion to diagnose LQTS is the LQTS “diagnostic score”. The score is calculated by assigning different points to various criteria (listed below). With four or more points, the probability is high for LQTS; with one point or less, the probability is low. A score of two or three points indicates intermediate probability.

*Family history (the same family member cannot be counted for LQTS and sudden death)
#Other family members with definite LQTS – 1 point
#Sudden death in immediate family (members before the age 30) – 0.5 pointsTreatment options:
Those diagnosed with long QT syndrome are usually advised to avoid drugs that would prolong the QT interval further or lower the threshold for TDP. In addition to this, there are two intervention options for individuals with LQTS: arrhythmia prevention and arrhythmia termination.

Arrhythmia prevention:
Arrhythmia suppression involves the use of medications or surgical procedures that attack the underlying cause of the arrhythmias associated with LQTS. Since the cause of arrhythmias in LQTS is after depolarizations, and these after depolarizations are increased in states of adrenergic stimulation, steps can be taken to blunt adrenergic stimulation in these individuals. These include:

*Administration of beta receptor blocking agents which decreases the risk of stress induced arrhythmias. Beta blockers are the first choice in treating Long QT syndrome.
In 2004 it has been shown that genotype and QT interval duration are independent predictors of recurrence of life-threatening events during beta-blockers therapy. Specifically the presence of QTc >500ms and LQT2 and LQT3 genotype are associated with the highest incidence of recurrence. In these patients primary prevention with ICD (Implantable cardioverter-defibrillator) implantation can be considered.

*Potassium supplementation. If the potassium content in the blood rises, the action potential shortens and due to this reason it is believed that increasing potassium concentration could minimize the occurrence of arrhythmias. It should work best in LQT2 since the HERG channel is especially sensitive to potassium concentration, but the use is experimental and not evidence based.

*Mexiletine. A sodium channel blocker. In LQT3 the problem is that the sodium channel does not close properly. Mexiletine closes these channels and is believed to be usable when other therapies fail. It should be especially effective in LQT3 but there is no evidence based documentation.

*Amputation of the cervical sympathetic chain (left stellectomy). This may be used as an add-on therapy to beta blockers but modern therapy mostly favors ICD implantation if beta blocker therapy fails.

Arrhythmia termination:
Arrhythmia termination involves stopping a life-threatening arrhythmia once it has already occurred. One effective form of arrhythmia termination in individuals with LQTS is placement of an implantable cardioverter-defibrillator (ICD). Alternatively, external defibrillation can be used to restore sinus rhythm. ICDs are commonly used in patients with syncopes despite beta blocker therapy, and in patients who have experienced a cardiac arrest.

It is hoped that with better knowledge of the genetics underlying the long QT syndrome, more precise treatments will become available.Prognosis:
The risk for untreated LQTS patients having events (syncopes or cardiac arrest) can be predicted from their genotype (LQT1-8), gender and corrected QT interval.

*High risk (>50%)
QTc>500 msec LQT1 & LQT2 & LQT3 (males)

*Intermediate risk (30-50%)
QTc>500 msec LQT3 (females)

QTc<500 msec LQT2 (females) & LQT3

*Low risk (<30%)
QTc<500 msec LQT1 & LQT2 (males)

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

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A study of 3,000 patients found that chest compressions alone increased chances of survival by more than 22%.

But training in how to give both chest compressions and mouth-to-mouth breaths is the best option, experts say.

The UK Resuscitation Council is due to produce new CPR guidelines next week.

Cardiopulmonary resuscitation (CPR) is a combination of chest compressions and mouth-to-mouth breaths, given in a life-threatening emergency like a cardiac arrest or heart attack.

The study, compiled by doctors from the Medical University of Vienna in Austria, looked at the survival rates of people treated by untrained members of the public taking instructions from the emergency services over the phone.

Dr Peter Nagele, from the department of anaesthesiology, critical care and pain therapy at the Medical University of Vienna, said that if untrained bystanders avoided mouth-to-mouth breaths during CPR, they were more likely to perform uninterrupted chest compressions.

That then increased the probability of CPR being successful.
Different techniques
The research in The Lancet involved two analyses.

The first used data from three randomised trials involving more than 3,000 patients.

It showed that chest-compression-only CPR was associated with a slightly improved chance of survival compared with standard CPR (14% v 12%).

In the second analysis of seven observational studies, researchers found no difference between the two CPR techniques.

Dr Jas Soar, chair of the Resuscitation Council from Southmead Hospital in Bristol, said: “Any CPR is better than no CPR. If you witness a cardiac arrest, dial 999 immediately. Those trained in CPR should follow existing guidance of 30 chest compressions followed by two rescue breaths.

“Those not trained should start compressions and follow instructions until an expert arrives,” Dr Soar said.

Dr Meng Aw-Yong, medical adviser at St John Ambulance, acknowledged that rescue breaths could be off-putting.

“The current advice is that if you’re unwilling or unable to do full CPR then chest compressions are better than nothing.

“The best solution, however, is for people to get trained in how to carry out chest compressions and rescue breaths so they can be the difference between a life lost and a life saved,” he said.

Claire O’Neill, community resuscitation programme lead at the BHF, said: “For someone who is untrained in cardiopulmonary resuscitation, doing both chest compressions and rescue breaths really can be difficult.

“We also know that uninterrupted chest compressions are very important for increasing the chance of survival. So being directed to focus solely on chest compressions could make people more willing to attempt resuscitation, which could ultimately save lives,” she said.

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Examination of 52 patients found levels of the body’s waste gas were higher in the 11 who reported such experiences, the journal Critical Care reports.

The Slovenian researchers hope to move on the debate over why so many cardiac arrest patients report the experences.

Reasons previously suggested for the phenomenon include religion and drugs.

Those who have had near-death experiences report various encounters, including seeing a tunnel or bright light, a mystical entity, or looking down from the ceiling at the scene below in an “out of body” experience.

Others describe a simple but overwhelming feeling of peace and tranquillity.

It is thought between one in ten and nearly a quarter of cardiac arrest patients have experienced one of these sensations.

No religion
In this latest study, published in the journal Critical Care, a team looked at 52 cardiac arrest patients. Eleven of these reported a near-death experience.

There appeared to be no pattern in regards to sex, religious belief, fear of death, time to recover or drugs given during resuscitation.

And while anoxia – in which brain cells die through lack of oxygen – is one of the principal theories as to why near-death experiences may occur, this was not found to be statistically significant among this small group of patients.

Instead, the researchers from the University of Maribor found blood carbon dioxide levels were significantly higher in the near-death group than among those who had no experience.

Previous research has shown that inhalation of carbon dioxide can induce hallucinatory experiences similar to those reported in near-death experiences.

Whether the higher levels of carbon dioxide among this group of patients were down to the cardiac arrest itself or pre-existing is unclear.

“It is potentially another piece of the puzzle, although much more work is needed,” said the report author, Zalika Klemenc-Ketis. “Near death experiences make us address our understanding of human consciousness so the more we know the better.”

Cardiologist Dr Pim van Lommel, who has studied near death experiences extensively, described the findings as “interesting”.

“But they have not found a cause – merely an association. I think this is something that will remain one of the great mysteries of mankind. The tools scientists have are simply not sufficient to explain it.”

In the UK, a large study is ongoing into whether cardiac arrest patients genuinely do have out-of-body experiences. The research includes placing images on shelves that can only be seen from above. The brain activity of 1,500 patients will be analysed afterwards to see if they can recognise the images.

Dr Sam Parnia, who is leading the project at Southampton University, says he hopes to establish whether consciousness can in fact exist as a separate entity to the body.

Zalika Klemenc-Ketis.. says… “Near death experiences make us address our understanding of human consciousness so the more we know the better ”

The researchers got permission to take samples of the muscles of women undergoing caesarean sections at the Royal Victoria Infirmary in Newcastle, the Cellular and Molecular Medicine journal reported.

Contractions
They exposed the muscle to TSA and measured the effects on both spontaneous contractions and those induced by the labour drug, oxytocin.

They found an average 46% reduction in contractions for the spontaneously contracting tissue and an average 54% reduction in the oxytocin induced contractions.

It has been previously shown that a protein kinase A (PKA) is involved in controlling the relaxation of the uterus during pregnancy.

The researchers showed that TSA increased the levels of a protein sub-unit of PKA.

Professor Nick Europe-Finner, who led the research, said: “We will not give this drug to a patient because it can damage as many as 10% of the genes in a cell.

“But it does show us that other more specific agents that act on the same enzymes but only one at a time are worth investigating.”

New treatment
Dr Yolande Harley, deputy director of research at Action Medical Research which funded the study, said: “This project has uncovered some of the molecular pathways that regulate uterine contractions and so could be linked to premature birth.

“It could have a role in preventing premature birth – finding a new treatment for early labour would be a major step forward.”

Professor Jane Norman, a spokeswoman for the Royal College of Obstetrics and Gynaecology (RCOG), said: “At the moment, it’s not possible to treat preterm labour effectively. We only have drugs that delay it by 24 hours or so – not enough to deliver the baby safely.

“One of the interesting things about this research is that they are using a new kind of drug – the drugs we are currently using have been around for a long time.

“And they are targeting pathways we have not known about before.

“When you consider that preterm birth rates are rising in all four countries of the UK a new more effective drug is badly needed.”